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Cecilia J. Hillard

Researcher at Medical College of Wisconsin

Publications -  272
Citations -  21171

Cecilia J. Hillard is an academic researcher from Medical College of Wisconsin. The author has contributed to research in topics: Endocannabinoid system & Cannabinoid receptor. The author has an hindex of 80, co-authored 250 publications receiving 18735 citations. Previous affiliations of Cecilia J. Hillard include Gulf Coast Regional Blood Center & United States Department of Veterans Affairs.

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Cannabinoid CB2 Receptors and Fatty Acid Amide Hydrolase Are Selectively Overexpressed in Neuritic Plaque-Associated Glia in Alzheimer's Disease Brains

TL;DR: Results show that both fatty acid amide hydrolase and cannabinoid CB2 receptors are abundantly and selectively expressed in neuritic plaque-associated astrocytes and microglia, respectively, whereas the expression of CB1 receptors remains unchanged.
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Endocannabinoid Signaling Negatively Modulates Stress-Induced Activation of the Hypothalamic-Pituitary-Adrenal Axis

TL;DR: Data indicate that e CB signaling negatively modulates HPA axis function in a context-dependent manner and suggest that pharmacological augmentation of eCB signaling could serve as a novel approach to the treatment of anxiety-related disorders.
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Modulation of the cannabinoid CB2 receptor in microglial cells in response to inflammatory stimuli

TL;DR: Data demonstrate that microglial cell activation is accompanied by CB2 receptor up‐regulation, suggesting that this receptor plays an important role in microglia cell function in the CNS during autoimmune‐induced inflammation.
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Inhibition of an equilibrative nucleoside transporter by cannabidiol: A mechanism of cannabinoid immunosuppression

TL;DR: It is demonstrated that CBD has the ability to enhance adenosine signaling through inhibition of uptake and provide a non-cannabinoid receptor mechanism by which CBD can decrease inflammation.
Journal Article

Synthesis and Characterization of Potent and Selective Agonists of the Neuronal Cannabinoid Receptor (CB1)

TL;DR: ACPA and ACEA are high-affinity agonists of the CB1 receptor but do not bind the CB2 receptor, suggesting that structural analogs of AEA can be designed with considerable selectivity for theCB1 receptor over theCB2 receptor.